Major advances in the field of multi-system biology have revolutionized the understanding of kidney, cardiac, and skeletal diseases in recent years. These advances are the basis for assembling a diverse group of investigators to discuss new scientific findings in kidney-bone and cardiovascular interactions. The objective being to initiate and direct progress towards treating and improving lives of patients with kidney and skeletal disorders. Kidney disease is a growing pandemic causing high rates of cardiovascular morbidity and mortality. In addition, many aging Americans have reduced kidney function as part of their aging kidney, and it is unclear whether the aging kidney contributes to the elevated risk of cardiovascular and skeletal disease in the elderly. Approximately 2 million fractures occur annually in the U.S. among those >50 years old with an estimated treatment cost of $17 billion, projected to increase by 50% by 2025. Thus, the burden of the syndromes caused by disordered kidney-bone and cardiovascular interactions to our society is huge, and scientific progress in the systems biology and pathobiology in these diseases lends new hope for novel diagnostic and therapeutic approaches and better quality of life. Kidney disease is the strongest risk factor for cardiovascular disease. All the kidney disease-specific cardiovascular risk factors to date are components of a syndrome, referred to as the chronic kidney disease-mineral bone disorder (CKD-MBD). Kidney disease associated osteoporosis is a component of this syndrome in addition to all the other skeletal derangement collectively known as renal osteodystrophy. Direct bidirectional interactions between the kidney and bone are known through the physiology of calcitriol and erythropoetin. However, the field of kidney-bone-cardiovascular interactions has made major recent strides. New hormones of both skeletal and renal origin acting on the other organs have been discovered since 2000 when FGF23 was discovered. FGF23, secreted by osteocytes, regulates renal phosphate excretion and calcitriol synthesis. FGF23 is dysregulated in CKD, and is a strong cardiovascular risk factor. Regulation of FGF23 secretion occurs in part through phosphorus, but many unknown factors still await discovery. Recently, soluble Klotho from the kidney has been shown to directly affect FGF23 secretion - a direct demonstration of the circulating functions of Klotho. Klotho is also associated with aging, osteoporosis, vascular calcification and cognitive impairment, besides its roles as a transmembrane protein which serves as a co-receptor for FGF23. New debate discussed in this proposed forum addresses the issue of direct actions and functions of Klotho independent of FGF23, versus its role as the FGF23 co-receptor. Actions of FGF23 as a direct cardiotoxin in CKD will be debated. The pathogenesis of the CKD-MBD related to the release of renal repair factors to the circulation and disordered phosphate homeostasis will be discussed along with current treatment recommendations beyond current guidelines. The meeting will be designed to foster interactions, promote collaboration and stimulate young investigators.